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Effect of postnecrotic and alcoholic hepatic cirrhosis on development of benign prostatic hyperplasia
M Cetinkaya1, H Cetinkaya, E Ulusoy
1Department of Urology, Ankara Numune Hospital, Turkey.
Background:
The object of this study was to investigate the effects of hepatic cirrhosis on the development of benign prostatic hyperplasia and consequent effects on prostatic volume, serum prostate-specific antigen (PSA), and prostatism symptoms.
Methods:
Sixty patients with postnecrotic cirrhosis and alcoholic cirrhosis at age 40 and over, and 20 voluntary subjects in the same age group with normal hepatic functions, were evaluated with prostatic volume calculation by transrectal ultrasound, symptom scoring according to American Urology Association (AUA) criteria, measurement of serum prostate-specific antigen (PSA), serum total testosterone (TT), free testosterone (FT), estradiol (E2), and calculation of E2/FT ratios, and the results were analyzed statistically by the Mann-Whitney U-test.
Results:
Serum FT and TT levels were significantly lower in the hepatic cirrhosis group compared to the control group (P = 0.0000 and P = 0000, respectively). Though mean serum E2 level was a little higher in cirrhotic patients compared to controls, the difference was not significant; however, the higher E2/FT ratio in the cirrhotic group was statistically significant (P = 0.27 and P = 0.0002, respectively). In the cirrhotic group, the decrease in FT and TT levels was greater, as the disease advanced. While E2 and E2/FT ratio increase, correlate with poor prognosis, no statistically significant differences were found. Mean prostatic volume, serum PSA level, and total symptom score were significantly higher in the control group, compared to the cirrhotic group (P = 0.0001, P = 0.0006, and P = 0.002, respectively). Prostatic volume decreased parallel to severity of disease in cirrhotic patients.
Conclusions:
The main reason for the decrease in mean prostatic volume in cirrhotic patients compared to subjects in the same age group with normal hepatic functions was the decrease in serum FT and TT levels, and the secondary cause was the increase in E2/FT ratio, indicating estrogenic predominance.